Oxygenated carotenoid lutein and progression of early atherosclerosis - The Los Angeles Atherosclerosis Study

被引:263
作者
Dwyer, JH
Navab, M
Dwyer, KM
Hassan, K
Sun, P
Shircore, A
Hama-Levy, S
Hough, G
Wang, XP
Drake, T
Merz, CNB
Fogelman, AM
机构
[1] Univ So Calif, Dept Prevent Med, Inst Prevent Res, Keck Sch Med, Los Angeles, CA 90089 USA
[2] Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA
[3] Univ Calif Los Angeles, Sch Med, Dept Lab & Expt Pathol, Los Angeles, CA USA
[4] Cedars Sinai Med Ctr, Dept Med, Div Cardiol, Los Angeles, CA 90048 USA
关键词
atherosclerosis; epidemiology; carotid arteries; ultrasonography; diet; lutein;
D O I
10.1161/01.CIR.103.24.2922
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-Carotenoids are hypothesized to explain some of the protective effects of fruit and vegetable intake on risk of cardiovascular disease. The present study assessed the protective effects of the oxygenated carotenoid lutein against early atherosclerosis. Methods and Results-Epidemiology: Progression of intima-media thickness (IMT) of the common carotid arteries over 18 months was determined ultrasonographically and was related to plasma lutein among a randomly sampled cohort of utility employees age 40 to 60 years (n=480). Coculture: The impact of lutein on monocyte response to artery wall cell modification of LDL was assessed in vitro by quantification of monocyte migration in a coculture model of human intima, Mouse models: The impact of lutein supplementation on atherosclerotic lesion formation was assessed in vivo by assigning apoE-null mice to chow or chow plus lutein (0.2% by weight) and LDL receptor-null mice to Western diet or Western diet plus lutein. IMT progression declined with increasing quintile of plasma lutein (P for trend=0.007, age-adjusted; P = 0.0007, multivariate). Covariate-adjusted IMT progression (mean +/- SEM) was 0.021+/-0.005 mm in the lowest quintile of plasma lutein, whereas progression was blocked in the highest quintile (0.004+/-0.005 mm; P=0.01). In the coculture, pretreatment of cells with lutein inhibited LDL-induced migration in a dose-dependent manner (P<0.05). Finally, in the mouse models, lutein supplementation reduced lesion size 44% in apoE-null mice (P=0.009) and 43% in LDL receptor-null mice (P=0.02). Conclusions-These epidemiological, in vitro, and mouse model findings support the hypothesis that increased dietary intake of lutein is protective against the development of early atherosclerosis.
引用
收藏
页码:2922 / 2927
页数:6
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